Biomarkers in the diagnostic algorithm of myalgic encephalomyelitis/chronic fatigue syndrome, 2022, Gravelsina et al

Biomarkers in the diagnostic algorithm of myalgic encephalomyelitis/chronic fatigue syndrome
Gravelsina Sabine, Vilmane Anda, Svirskis Simons, Rasa-Dzelzkaleja Santa, Nora-Krukle Zaiga, Vecvagare Katrine, Krumina Angelika, Leineman Iana, Shoenfeld Yehuda, Murovska Modra

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex disease that is mainly diagnosed based on its clinical symptoms. Biomarkers that could facilitate the diagnosis of ME/CFS are not yet available; therefore, reliable and clinically useful disease indicators are of high importance. The aim of this work was to analyze the association between ME/CFS clinical course severity, presence of HHV-6A/B infection markers, and plasma levels of autoantibodies against adrenergic and muscarinic acetylcholine receptors.

A total of 134 patients with ME/CFS and 33 healthy controls were analyzed for the presence of HHV-6A/B using PCRs, and antibodies against beta2-adrenergic receptors (β2AdR) and muscarinic acetylcholine receptors (M3 AChR and M4 AChR) using ELISAs. HHV-6A/B U3 genomic sequence in whole-blood DNA was detected in 19/31 patients with severe ME/CFS, in 18/73 moderate ME/CFS cases, and in 7/30 mild ME/CFS cases. Severity-related differences were found among those with a virus load of more than 1,000 copies/1,000,000 PBMCs.

Although no disease severity-related differences in anti-β2AdR levels were observed in ME/CFS patients, the median concentration of these antibodies in plasma samples of ME/CFS patients was 1.4 ng/ml, while in healthy controls, it was 0.81 ng/ml, with a statistically significant increased level in those with ME/CFS (p = 0.0103). A significant difference of antibodies against M4 AChR median concentration was found between ME/CFS patients (8.15 ng/ml) and healthy controls (6.45 ng/ml) (p = 0.0250). The levels of anti-M4 plotted against disease severity did not show any difference; however, increased viral load correlates with the increase in anti-M4 level.

ME/CFS patients with high HHV-6 load have a more severe course of the disease, thus confirming that the severity of the disease depends on the viral load—the course of the disease is more severe with a higher viral load. An increase in anti-M4 AchR and anti-β2AdR levels is detected in all ME/CFS patient groups in comparison to the control group not depending on ME/CFS clinical course severity. However, the increase in HHV-6 load correlates with the increase in anti-M4 level, and the increase in anti-M4 level, in turn, is associated with the increase in anti-β2AdR level. Elevated levels of antibodies against β2AdR and M4 receptors in ME/CFS patients support their usage as clinical biomarkers in the diagnostic algorithm of ME/CFS.

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Fukuda

 

"ME/CFS patients with high HHV-6 load have a more severe course of the disease, thus confirming that the severity of the disease depends on the viral load—the course of the disease is more severe with a higher viral load."

Or the immune system of someone who is less well will find it harder to control or eliminate infections that are potentially secondary.

 

Indeed. Much of the science that gets posted here is shockingly bad, isn't it?

 

Sadly, yes. But if we, at least, don't point that out there is little counterpoint to the almost inevitable hype.

 

I think its worse than just its bad. A lot of it is on already discredited approaches and the only way to get them to show a result is to set the study up with a lot of bias, looks like intentional fraud. The studies in progress don't look any better, NICE 2021 hasn't changed much.

 

If 23/30 mild cases didn't show the virus, then maybe it's not part of ME? My guess is that any immune system activation, from viral infections, tissue damage, or whatever else, will increase the severity of ME symptoms. It's just an extra load on top of ME's symptoms due to the immune system not working properly.

They should take the evidence that people can have ME without any of the viral infections that they keep studying (because it's easy to do and get funding for?) and stop funding ME research based on viral infection.